| Lead Exposure Is Associated with Decreased Serum Paraoxonase 1 (PON1) Activity and Genotypes Wan-Fen Li,1 Mei-Hung Pan,2 Meng-Chu Chung,1 Chi-Kung Ho,3 and Hung-Yi Chuang2,3 1Division of Environmental Health and Occupational Medicine, National Health Research Institutes, Zhunan, Taiwan; 2Graduate Institute of Public Health, College of Health Sciences, Kaohsiung Medical University, Kaohsiung, Taiwan; 3Department of Occupational Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
Abstract
Lead exposure causes cardiac and vascular damage in experimental animals. However, there is considerable debate regarding the causal relationship between lead exposure and cardiovascular dysfunction in humans. Paraoxonase 1 (PON1) , a high-density lipoprotein-associated antioxidant enzyme, is capable of hydrolyzing oxidized lipids and thus protects against atherosclerosis. Previous studies have shown that lead and several other metal ions are able to inhibit PON1 activity in vitro. To investigate whether lead exposure has influence on serum PON1 activity, we conducted a cross-sectional study of workers from a lead battery manufactory and lead recycling plant. Blood samples were analyzed for whole-blood lead levels, serum PON1 activity, and three common PON1 polymorphisms (Q192R, L55M, –108C/T) . The mean blood lead level (± SD) of this cohort was 27.1 ± 15 µg/dL. Multiple linear regression analysis showed that blood lead levels were significantly associated with decreased serum PON1 activity (p < 0.001) in lead workers. This negative correlation was more evident for workers who carry the R192 allele, which has been suggested to be a risk factor for coronary heart disease. Taken together, our results suggest that the decrease in serum PON1 activity due to lead exposure may render individuals more susceptible to atherosclerosis, particularly subjects who are homozygous for the R192 allele. Key words: atherosclerosis, lead, metal, paraoxonase, polymorphism. Environ Health Perspect 114:1233–1236 (2006) . doi:10.1289/ehp.9163 available via http://dx.doi.org/ [Online 18 May 2006]
Address correspondence to H.-Y. Chuang, Kaohsiung Medical University Hospital, 100 Shih-Chuan 1st Rd., San Ming District, Kaohsiung 80708, Taiwan. Telephone: 886-7-311-5974. Fax: 886-7-311-5948. E-mail: ericch@cc.kmu.edu.tw We thank the workers and employers for their cooperation. This work was supported by the National Health Research Institutes (grants EO-093-PP-09, EO-093-PP-10) and the National Science Council (grant NSC 93-2320-B-037-019) of Taiwan. The contents are solely the responsibility of the authors and do not necessarily represent the official view of the National Health Research Institutes of Taiwan. The authors declare they have no competing financial interests. Received 14 March 2006 ; accepted 18 May 2006.
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